Chicken lncRNA-9802 Induces the S Phase Arrest in the T Lymphocyte Cells Infected by Marek’s Disease Virus via the TP53BP1/p53/p21 Pathway
by
Shuo Han
1,2,†,
Haile Ren
2,†,
Jingyi Yang
2,†,
Kexin Han
2,
Yunqiao Qiu
1,2,
Yingxue Jiang
2,
Limei Han
2,* and
Liping Han
3,* 1
Engineering Laboratory for Tarim Animal Diseases Diagnosis and Control, College of Animal Science and Technology, Tarim University, Alar 843300, China
2
Key Laboratory of Livestock Infectious Diseases in Northeast China, Ministry of Education, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China
3
Department of Bioscience, Changchun Normal University, Changchun 130032, China
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Vet. Sci. 2026, 13(5), 469; https://doi.org/10.3390/vetsci13050469
Submission received: 15 April 2026
/
Revised: 5 May 2026
/
Accepted: 9 May 2026
/
Published: 12 May 2026
Simple Summary
Marek’s disease represents a significant viral pathology characterized by tumor formation in chickens, which detrimentally impacts poultry health on a global scale. This study explored the role of lncRNA-9802 in the proliferation of Marek’s disease virus-infected T cells, which exhibits elevated expression levels in the chicken spleen following infection with the Marek’s disease virus. Our findings indicate that increased levels of lncRNA-9802 disrupt the proliferation of these infected T cells by causing cell cycle arrest at the S phase. This arrest is mediated through a signaling cascade involving three key proteins, which subsequently modulate the expression of proteins governing the cell cycle. These findings contribute to the identification of novel therapeutic targets for Marek’s disease, facilitating the advancement of antiviral strategies.
Abstract
The oncogenic Marek’s disease virus (MDV) triggers Marek’s disease (MD), which is a substantial threat to poultry as it transforms infected T cells into tumors. Our research identified that long non-coding RNA 9802 (lncRNA-9802) exhibits increased expression in the chicken spleen following MDV infection, with its expression being strongly associated with the expression of tumor p53-binding protein 1 (TP53BP1). The function of lncRNA-9802 in T cells transformed by MDV remains unclear. Consequently, the expression levels of lncRNA-9802 were either over-expressed or knocked down in MDV-transformed T cells, MDCC-MSB1, through lentivirus-mediated over-expression and knock down experiments. Our findings demonstrate that lncRNA-9802 induces proliferation disturbances in MDCC-MSB1 cells by causing arrest in the S phase, which is accompanied by increased expression levels of TP53BP1, p53, and p21. Activation of the p53 pathway results in elevated levels of Cyclin E and Cyclin-dependent kinase 2 (CDK2), thereby facilitating the entry of MDCC-MSB1 cells into the S phase. Concurrently, the reduced levels of Cyclin A inhibit the exit of MDCC-MSB1 cells from the S phase. By modulating the TP53BP1/p53/p21 pathway, lncRNA-9802 induces S phase arrest in MDCC-MSB1 cells, characterized by upregulation of Cyclin E and CDK2 and downregulation of Cyclin A. This research enhances the understanding of the pathogenic mechanisms of MDV and provides a foundation for identifying potential targets for antiviral drug development.
Keywords:
Marek’s disease virus; lncRNA-9802; TP53BP1; cell cycle; S phase arrest
